肝硬化患者消化道状态与血氨的关系研究

目的研究肝硬化伴消化道功能障碍患者酸化肠道治疗前、后的血氨水平变化,探讨肝硬化患者消化道状态与血氨水平的关系,寻找减少肠道氨吸收的有效方法,达到降低血氨的目的。方法测定195例肝硬化患者(包括单纯性肝硬化患者100例、肝硬化伴消化道出血患者52例、肝硬化伴便秘患者43例)、50例单纯性肠梗阻患者、113例单纯性消化道出血患者及80名正常对照者的空腹血氨水平。比较各组血氨水平,研究肝硬化伴消化道出血或(和)便秘患者酸化肠道治疗前、后的血氨水平变化。结果肝硬化伴消化道出血组血氨水平为(67.71±30.31)μmol/L,高于单纯性肝硬化组[(45.81±28.78)μmol/L]、单纯性消化道出血组[(24.85±10.79)μmol/L]和正常对照组[(22.42±7.93)μmol/L](P<0.05)。肝硬化伴便秘组血氨水平为(95.53±42.61)μmol/L,高于单纯性肝硬化组、肝硬化伴消化道出血组和单纯性肠梗阻组[(24.90±11.02)μmol/L](P<0.05)。单纯性肝硬化组血氨水平高于单纯性消化道出血、单纯性肠梗阻组及正常对照组(P<0.05);而单纯性消化道出血、单纯性肠梗阻组与正常对照组比较差异无统计学意义(P>0.05)。肝硬化伴消化道出血或(和)便秘组治疗前血氨水平为(83.28±37.93)μmol/L,明显高于经酸化肠道治疗后的血氨水平[(50.89±19.58)μmol/L](P<0.05)。结论肝硬化患者消化道状态与血氨水平关系密切;阻止消化道出血、酸化肠道及使用抗生素可抑制肠道中氨的产生和吸收,从而降低血氨水平,预防和治疗肝性脑病。     

血氨对亚临床肝性脑病的影响

目的：观察不同的亚临床肝性脑病(SHE)诊断标准下慢性肝病患者的血氨水平，探讨血氨与SHE的关系。方法：对126例慢性肝病患者进行血氨、数字连接试验(NCT)、数字符号试验(Nsy)检测，其中32例做脑干听觉诱发电位(BAEP)检查，观察比较SHE组与非SHE组血氨水平的差异。结果：肝硬化组血氨水平高于非肝硬化组(P＝0．0002)；同时肝硬化组的SHE发生率(22／49；44．90％)高于非肝硬化组(20/77；25．97％)，差异有统计学意义(P=0．028)。肝硬化病人以NCT异常为诊断标准的SHE组血氨水平高于非SHE组(P＜0．05)，但非肝硬化组则差异无统计学意义(P＞0．05)；而以Nsy、NCT和(或)BAEP异常为诊断标准的SHE组与非SHE组的血氨水平比较差异无统计学意义(P＞0．05)；以BAEP异常为诊断标准的SHE组血氨值却低于非SHE组(P＜0．05)。结论：血氨不能作为SHE的诊断标准，但血氨对肝硬化病人以NU异常为诊断标准的SHE的产生及进展可能有一定的关系。     

根除幽门螺杆菌对肝硬化患者血氨浓度的影响

目的观察肝硬化合并感染幽门螺杆菌（Hp）患者根除幽门螺杆菌前后血氨浓度的变化。方法确诊的肝硬化住院患者116例,Hp阴性患者设为A组（40例）,Hp阳性（76例）患者随机分为B组（40例）,C组（36例）。三组行护肝治疗和降血氨的标准化治疗,C组在此基础上再加上幽门螺杆菌根除治疗,三组治疗时间为2周,治疗前、治疗1周后、治疗2周后分别测空腹血氨值。结果 Hp感染与血氨浓度关系：阳性组血氨（85.3±25.8）μmol/L浓度高于阴性组（62.9±24.0）μmol/L,差异无显著性（P〉0.05）。Hp治疗前后血氨浓度变化：阳性组76例根除2周后66例转阴,治疗前血氨与治疗后血氨（57.6±27.1）μmol/L比较,差异有显著性（P〈0.05）。Hp感染对不同肝功能期血氨的影响：阳性组76例按Child分级,A级、B级、C级三组之间血氨值比较,差异有显著性（P〈0.05）。阴性组A级、B级、C级之间血氨值比较,差异无显著性（P〉0.05）。结论肝硬化合并感染幽门螺杆菌患者在对其肝硬化常规治疗的同时根除幽门螺杆菌有助于降低血氨浓度,降低患肝性脑病的风险。     

根除Hp对肝硬化血氨的影响与肝功能分级的关系

目的 探讨根除Hp对肝硬化血氨的影响与肝功能分级的关系。方法回顾分析80例患者的临床资料。结果治疗前Hp阳性组血氨浓度为（81．5±21．5）μmol／L,比Hp阴性组（35．8±16．2）izmoL／L明显增高,经检验两者差异有统计学意义（P〈0．05）,Hp阴性组与对照组（35．5±13．0）μmol／L比较差异无统计学意义（P〉0．05）。治疗后Hp阳性组Hp仍阳性的2例,血氨浓度为（59．3±11．1）μmol／L,转阴33例,血氨浓度为（35．5±12．0）μmol／L;Hp阴性组血氨浓度为（36．0±14．0）μmol／L;对照组Hp仍阳性的2例,血氨浓度为（35．0±12．0）μmol／L,转阴38例,血氨浓度为（34．2±13．0）μmol／L。Hp阳性组治疗后仍阳性者血氨浓度屁著高于转阴者,其差异有统计学意义（P〈0．05）。Hp阳性组转阴者及Hp阴性组与对照组比较,差异无统计学意义（P〉0．05）。结论对肝硬化高血氨患者,特别是疑有肝性脑病,若常规降氨处理效果不佳时,应考虑是否合并Hp感染,并及时给予抗Hp治疗。肝硬化血氨升高患者在传统降氨治疗同时,应检测Hp感染情况。根除Hp有助降氨,可降低肝性脑病的发生,具有重要临床意义。     

经颈静脉肝内门体分流术对肝硬化患者血氨水平的影响

目的:比较肝硬化患者经颈静脉肝内门体分流术(transjugular intrahepatic portosystemic shunt,TIPS)前后的血氨水平和实验室指标,探讨TIPS对肝硬化患者血氨水平的影响,明确TIPS与肝性脑病的关系.方法:纳入我院2009年1月至2010年12月行TIPS治疗的肝硬化患者66例,于术前1d、术后第3天及出院时三次测定患者肝肾功能、电解质指标及血氨,比较患者术前和术后实验室指标的差异,血氨水平变化和肝性脑病的发生情况.结果:TIPS术前1d的血氨水平为(37.3±21.6) μmol/L,术后第3天和出院时血氨水平分别为(52.3±27.3)μmol/L和(65.1±39.8)μmol/L,均高于术前(t值分别为-2.116和-3.903,P＜0.05);TIPS术前无肝性脑病发生,术后出现6例Ⅰ型肝性脑病患者.结论:肝硬化患者TIPS术后血氨水平升高,TIPS有促进肝性脑病发生的可能.     

肝肾综合征与肝性脑病的关系研究

目的分析慢性重型肝炎伴肝肾综合征(HRS)患者的血氨水平及肝性脑病(HE)发生率,探讨HRS与HE的关系。方法纳入我院2008年1月至2010年10月因慢性重型肝炎住院患者450例,根据患者在住院期间是否发生HRS,分成HRS组(病理组,105例)和非HRS组(病理对照组345例),测定两组的生化指标和血氨,并统计两组HE发生率和分级。结果 HRS组血氨水平为78.4±25.6μmol/L,高于非HRS组的48.3±18.7μmol/L(t=2.68,P<0.05)。HRS组中有47例发生HE(分级为HEI12例、HEII16例、HEIII10例、HE IV9例),发生率为44.7%,高于非HRS组的34例(HEI 13例、HEII 9例、HEIII 8例、HEIV 4例),发病率为9.8%(χ2=64.45,P<0.05)。HRS组MELD、TB、DB、BU、CREA的水平分别为34.7±4.5、431.1±211.9μmol/L、319.2±157.3μmol/L、19.2±6.6mmol/L、258.2±115.1μmol/L,高于非HRS组的26.3±6.8、249.2±205.3μmol/L、180.1±140.3μmol/L、4.0±1.2mmol/L、75.4±18.1μmol/L(t值分别为2.45、3.75、3.65、11.47、7.86、1.51,P<0.05);GGT、ALP、K结果差异无统计学意义(P>0.05)。结论慢性重型肝炎患者并发HRS加重血氨水平升高,促进HE的发生和发展。     

肝硬化合并Hp感染测定血氨浓度的临床意义

目的探讨肝硬化患者合并幽门螺杆菌(Helicobacter pylori,Hp)感染后的血氨浓度变化与不同肝功能分级及门脉高压程度的关系,同时观察根除Hp后对血氨的影响.方法48例确诊为Hp阳性的肝硬化患者为阳性组,另有36例Hp阴性的肝硬化患者为阴性组,同时有40例Hp阳性的正常人为对照组;分别检测3组的血氨浓度进行比较,并应用丽珠胃三联治疗1周,于4周后再测定3组血氨浓度进行比较.结果阳性组的血氨浓度与阴性组和正常组相比有显著差异(P＜0.05);阴性组与对照组相比无显著差异(P＞0.05);阳性组不同肝功能分级组血氨浓度之间有显著差异(P＜0.01);而阳性组和阴性组食管静脉曲张不同程度之间的血氨浓度亦有显著差异(P＜0.01);治疗后3组的血氨浓度无显著差异(P＞0.05).结论Hp感染与肝硬化的血氨升高有密切相关性;而根除Hp可使血氨水平有显著降低.     

不稳定型心绞痛患者高半胱氨酸内皮素及血纤肽A的变化及意义

目的:探讨不稳定型心绞痛(unstable angina pectoris,UAP)患者血中高半胱氨酸(homocysteine,HCY)、内皮素及血纤肽A的变化及意义.方法:正常组31名,UAP患者40例根据入院前有无用药分为用药组21例和未用药组19例,分别测定血中HCY、内皮素及血纤肽A值.结果:UAP患者用药组、未用药组的HCY为[(12±5、12±6)μmol/L],内皮素为[(110±24、129±26)ng/L),血纤肽A为[(7.7±2.0、8.8±2.2)μg/L],均较正常组的HCY[(4.4±1.1)μmol/L],内皮素[(65±14)ng/L],血纤肽A[(3.5±0.6)μg/L]明显增高(P＜0.05),用药组与未用药组上述指标比较差异均无统计学意义(P＞0.05),UAP患者的HCY与内皮素水平呈正相关(r=0.4,P＜0.05).结论:HCY、内皮素及血纤肽A水平的改变可能参与了UAP的病理生理过程.     

四川高原地区H型高血压不同危险分层与血Hcy的相关性分析

目的探讨高原地区H型高血压患者血同型半胱氨酸(Hcy)与高血压危险分层的相关性。方法用循环酶法测定783例高血压Ⅱ、Ⅲ级患者(高血压组)及188例体检健康者(健康对照组)血Hcy水平,分析Hcy与高血压、性别、年龄段的关系。结果高血压组Ⅱ级[(17.4±4.3)μmol/L]与Ⅲ级[(22.3±6.8)μmol/L]血清Hcy水平均明显高于健康对照组[(12.6±2.3)μmol/L],且高血压Ⅲ级明显高于高血压Ⅱ级血清Hcy水平(P0.05);高血压Ⅱ级和Ⅲ级中男性血清Hcy水平[(19.4±5.2)μmol/L、(25.6±7.9)μmol/L]均明显高于女性血清Hcy水平[(15.1±3.4)μmol/L、(20.2±6.2)μmol/L](P0.05);在高血压Ⅲ级患者中60岁以上患者血清Hcy水平[(26.4±7.5)μmol/L]明显高于60岁以下患者血清Hcy水平[(19.5±5.4)μmol/L](P0.05)。结论血Hcy水平与高血压危险分层呈正相关性;男性患者Hcy水平明显高于女性;测定Hcy对预防及治疗H型高血压疾病有重要的临床意义。     

滴液式灌肠器的设计及临床应用

目的 评价自行设计滴液式灌肠器的应用效果.方法 自行设计滴液式灌肠器,将60例需行保留灌肠的Ⅱ级肝性脑病患者随机分为2组,观察组采用滴液式灌肠器灌肠;对照组使用传统的开放式袋状灌肠器灌肠,比较2组灌肠液保留时间、灌肠前后血氨浓度、药液外溢情况、患者满意度.结果 观察组、对照组灌肠液在肠腔内保留时间分别为(9.0±2.5)、(42.6±3.7)min,有显著性差异(P＜0.01);2组灌肠前血氨浓度分别为(105.2±15.4)、(103.6±14.3)μmol/L,无显著性差异(P＞0.05),2组灌肠后血氨浓度分别为(59.5±10.1)、(94.7±8.8)μmol/L,有显著性差异(P＜0.01);2组灌肠过程中药液外溢发生率分为0、73.3%,有显著性差异(P＜0.01);2组患者的满意度分别为93.3%、70.0%,有显著性差异(P＜0.05).结论 应用滴液式灌肠器保留灌肠可延长药物在肠腔内的保留时间,明显减少灌肠过程中药液外溢,有效提高治疗效果,同时可减轻患者的痛苦.     

肝功能衰竭肝性脑病大鼠5-羟色胺和去甲肾上腺素的变化

目的研究5-羟色胺(5-HT)及去甲肾上腺素(NA)在大鼠急性肝功能衰竭(ALF)和慢性肝功能衰竭(CLF)肝性脑病时的变化。方法将110只SD大鼠随机分为正常对照组(20只)、ALF组(45只)及CLF组(45只)。ALF模型按500mg/kg硫代乙酰胺(TAA)间隔24h两次灌胃;CLF模型按质量分数为0.03%的TAA作为饮用水灌饲10周,并根据每周体重的变化增减50%的TAA含量。造模成功后从眼底静脉丛取血,检测5-HT、NA、血氨和肝功能指标;处死动物,取肝、脑组织,光镜下观察组织病理学变化。结果ALF组和CLF组均出现不同程度的肝功能损害表现,血中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆红素(TBIL)、白蛋白(ALB)、白蛋白/球蛋白(A/G)、血氨均有明显变化(P<0.05或P<0.01);肝脏及脑组织病理学符合ALF和CLF肝性脑病表现。ALF组和CLF组5-HT(16.06±1.08)μmol/L和(15.32±1.48)μmol/L均较正常对照组(2.75±0.26)μmol/L显著升高(P均<0.01),CLF组NA值下降(94.0±2.13)pmol/L比(121.2±14.8)pmol/L,P<0.05。结论5-HT在大鼠ALF和CLF所致肝性脑病时明显升高;NA在大鼠CLF所致肝性脑病时明显下降。     

纳洛酮治疗肝硬化亚临床型肝性脑病疗效观察

目的：评估纳洛酮治疗肝经亚临床型肝性脑（ＳＨＥ）的疗效。方法：４７例ＳＨＥ随机分为治疗组２４例（Ａ组）,对照组２３例（Ｂ组）。双盲法分别给予治疗组纳洛酮０．４ｍｇ（１ｍＬ）、对照组０．９％氯化钠１ｍＬ,均１日１次肌肉注射,连用１０日。用药前后分别行数字连接试验９ＮＣＴ）、数字符合试验（ＤＳ）检测及测定血氨,并随访有否发生临床型肝性脑病。结果：治疗组治疗后ＮＣＴ、ＤＳ均比治疗前明显改善,Ｐ〈０．０１     

Subclinical hepatic encephalopathy: role of tryptophan binding to albumin and the competition with indole-3-acetic acid.

BACKGROUND: The role of tryptophan (TRY) and its metabolites in the pathogenesis of hepatic encephalopathy is conflicting. The aim of the present study is to investigate in posthepatitis cirrhotic patients with encephalopathy the serum levels of TRY and those of its metabolite indole-3-acetic acid, as well as TRY binding curve to serum albumin and the competition with indole-3-acetic acid. The presence of a relationship between encephalopathy severity and circulating free TRY was also investigated. METHODS: Serum TRY and indole-3-acetic acid were analyzed by HPLC; binding of TRY to serum albumin and the competition with indole-3-acetic acid was studied by equilibrium dialysis. RESULTS: Serum-free TRY was significantly higher in cirrhotic patients (43.33 +/- 14.70 vs 28.87 +/- 8.77 mumol/L, P = 0.02). The binding capacity of albumin was reduced in cirrhotics and further decreased by the addition of indole-3-acetic (K = 6.63 +/- 0.97 x 10(3) mol/L-1, gamma = 1.16 +/- 0.45 x 10(2) mol/L-1 in normal sera vs K = 1.04 +/- 0.20 x 10(3) mol/L-1, gamma = 1.91 +/- 0.92 10(2) mol/L-1 in cirrhotic sera). A multivariate analysis showed that among the psychometric tests the only independent predictor of serum levels of free TRY was the Block Design (R2 = 0.94, B = 0.16 +/- 0.01, beta = 0.97; P < 0.0001). CONCLUSIONS: A high percent ratio of free/total TRY and indoleacetic acid (IAA) was found in cirrhotic patients with hepatic encephalopathy. The concentrations of serum-free IAA and TRY correlated with the degree of subclinical encephalopathy, suggesting a role of these compounds in the development of mental derangement in liver cirrhosis.     

Evaluation of plasma ammonia levels in patients with acute liver failure and chronic liver disease and its correlation with the severity of hepatic encephalopathy and clinical features of raised intracranial tension

OBJECTIVES: The present study was designed to (a) evaluate and compare plasma ammonia levels (PAL) in patients with acute liver failure (ALF) and chronic liver disease (CLD) with or without hepatic encephalopathy (HE); (b) correlate the severity of HE with PAL; and (c) correlate PAL with clinical features of raised intracranial tension in ALF. DESIGN AND METHODS: A total of 40 patients, comprised of 20 patients with ALF (Group A) and 20 patients with CLD (Group B, which was comprised of 8 patients with HE (subgroup B1) and 12 patients without HE (subgroup B2)), were studied. PAL was estimated using an enzymatic UV-method (RANDOX). The clinical and biochemical profile of all the patients was recorded. Correlation between the grade of HE and PAL was derived using Pearson's correlation coefficient. The mean PAL of ALF patients with and without raised intracranial tension was compared using the standard error of difference between the two means. RESULTS: The mean PAL (micromol/L) +/- SD was as follows: Group A: 172.1 +/- 52.55, subgroup B1: 58.75 +/- 29.38, subgroup B2: 42.17 +/- 18.19 (normal levels = 10-47 micromol/L). All patients with ALF showed PAL more than the upper limit of the normal range, and there was good correlation between the severity of HE and PAL [r = 0.91 at P < 0.05]. In subgroup B1 (CLD with HE), 3/8 patients (37.5%), and in subgroup B2 (CLD with HE), 4/12 patients (33.3%) patients had PAL more than the upper limit of normal range. Within Group A, 14 patients had clinical features of raised intracranial tension/cerebral edema, and the mean PAL of these patients (188.21 +/- 49.15 micromol/L) was significantly higher than those who did not have features of raised intracranial tension (134.5 +/- 42.36 micromol/L) (SE of difference between two means). CONCLUSIONS: Raised PAL appears to be an important laboratory abnormality seen in patients with ALF, and there seems to be a significant correlation between the severity of encephalopathy and PAL in these patients. However, among patients with CLD, the proportion of patients with PAL more than the upper limit of normal range is not significantly different between those with or without HE. Our study also suggests that high PAL in ALF patients appears to correlate with clinical features of cerebral edema and raised intracranial tension.     

乳果糖治疗亚临床肝性脑病不同疗程的疗效观察

目的　观察乳果糖对亚临床肝性脑病 (SHE)不同疗程的疗效。方法　经数字连接试验 (NCT)和脑干听觉诱发电位 (BAEPs)诊断的SHE患者 86例 ,随机分为对照A组 2 2例 ,治疗B组 2 1例、C组 2 2例、D组 2 1例 ;对照组予常规护肝治疗 ,治疗组在对照组治疗的基础上予以乳果糖口服治疗 ,疗程分别为 4周、8周、12周 ,治疗前后每 2周予血氨、NCT和BAEPs检测。结果　疗程结束治疗组与对照组比较 ,血氨水平改善明显 (P <0 .0 1) ,BAEPs异常率降低 (P <0 .0 1) ,各组转为肝性脑病 (HE)的例数分别为A组 5例、B组 4例、C组 3例和D组 1例 ,C、D组转为HE的病例数明显少于A组 (P <0 .0 1) ;B组、C组停用乳果糖后出现了血氨上升 ,BAEPs异常率增加 ,转为HE的病例数明显多于D组。结论　乳果糖是治疗SHE的有效药物 ,长期治疗能够降低血氨 ,改善NCT ,降低HE的患病率     

幽门螺杆菌感染对血氨浓度的影响

目的　探讨消化系统疾病中幽门螺杆菌 (HP)感染对患者血氨浓度变化的影响。方法　分别用全自动生化仪及尿素酶依赖性试验对 75例消化性溃疡患者的血氨浓度及HP感染情况进行动态观察。结果　HP阳性组入院时的血氨浓度明显高于HP阴性组和HP阳性组根除治疗后的血氨浓度 (P <0 .0 1) ;HP阴性组 2次血氨测定结果差异无显著性 (P >0 .0 5 )。HP阳性组中HP根除治疗结束时有 4例患者血氨浓度由入院时的正常范围转为增高 ,两者差异有显著性 (P <0 .0 1)。 3例合并肝硬化患者 ,经护肝与降血氨等治疗 ,血氨未下降 ;后经胃镜检查证实分别合并胃溃疡 1例、十二指肠球部溃疡 2例 ,检查HP均呈阳性 ,经应用PPI三联根除治疗 ,疗程 1周 ,其血氨均下降至正常。结论　HP感染能导致血氨浓度增高 ,可能为肝性脑病的诱因之一。肝硬化伴有上消化道出血病 ,若同时有HP感染 ,在HP根除治疗前 ,如静脉持续应用PPI等强效制酸剂 ,可较长时间引起胃内 pH值 >6 ,从而使胃内氨向血中弥散 ,有诱发或加重肝性脑病的可能 ,应引起临床医师的重视     

Relationship between tumor necrosis factor-alpha and ammonia in patients with hepatic encephalopathy due to chronic liver failure

BACKGROUND: We have recently demonstrated that in humans, circulating levels of tumor necrosis factor-alpha (TNF) correlate positively with severity of hepatic encephalopathy (HE) due to chronic liver failure.AIM. The main aim of this larger population study is to determine the relationship between TNF and ammonia in patients with HE and chronic liver failure due to liver cirrhosis. METHODS: Circulating levels of TNF and ammonia were measured in 108 patients with liver cirrhosis due to various etiologies in various clinical grades of HE (grades 0-4). TNF concentrations were measured in venous serum using commercially available solid-phase high sensitivity enzyme-linked immunosorbent assay. Ammonia levels were determined in venous plasma by the enzymatic method, using the glutamate dehydrogenase reaction. RESULTS: The mean+/-SEM values of circulating levels of TNF and ammonia at presentation in patients with grade 0 of HE (n = 30) were 3.89+/-0.2 pg/mL and 49.8+/-2.8 microg/mL respectively, in patients with grade 1 of HE (n = 26) were 8.56+/-0.34 pg/mL and 101.6+/-6.5 microg/mL respectively, in patients with grade 2 of HE (n = 22) were 11.59+/-0.48 pg/mL and 160.3+/-10.7 microg/mL respectively, in patients with grade 3 of HE (n = 20) were 19.98+/-0.94 pg/mL and 228.8+/-16.1 microg/mL respectively, and in patients with grade 4 of HE (n = 10) were 51.53+/-8.59 pg/mL and 284.2+/-20.3 microg/mL respectively. A significant positive correlation was found between circulating levels of TNF and those of ammonia (r = 0.62, P< 0.0001), and also between circulating levels of both substances and severity of HE in these patients (r = 0.95, P<0.0001, and r = 0.9, P<0.0001 respectively). TNF and ammonia were both significant independent predictors of severity of HE (P<0.0001 for both variables). CONCLUSION: The results of this study demonstrate a significant relationship between TNF and ammonia in patients with chronic liver failure and HE, and so strengthen the suggestion that TNF could be strongly involved in the pathogenesis of HE in these patients. Hence, we suggest a new theory in the pathogenesis of HE, the "TNF theory".     

Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression.

Insulin secretion and insulin sensitivity were evaluated in eight clinically stable cirrhotic patients and in 12 controls. OGTT was normal in cirrhotics but plasma insulin response was increased approximately twofold compared with controls. Subjects received a three-step (0.1, 0.5, 1.0 mU/kg.min) euglycemic insulin clamp with indirect calorimetry, [6-3H]-glucose, and [1-14C]-palmitate. During the two highest insulin infusion steps glucose uptake was impaired (3.33 +/- 0.31 vs. 5.06 +/- 0.40 mg/kg.min, P less than 0.01, and 6.09 +/- 0.50 vs. 7.95 +/- 0.52 mg/kg.min, P less than 0.01). Stimulation of glucose oxidation by insulin was normal; in contrast, nonoxidative glucose disposal (i.e., glycogen synthesis) was markedly reduced. Fasting (r = -0.553, P less than 0.01) and glucose-stimulated (r = -0.592, P less than 0.01) plasma insulin concentration correlated inversely with the severity of insulin resistance. Basal hepatic glucose production was normal in cirrhotics and suppressed normally with insulin. In postabsorptive state, plasma FFA conc (933 +/- 42 vs. 711 +/- 44 mumol/liter, P less than 0.01) and FFA turnover (9.08 +/- 1.20 vs. 6.03 +/- 0.53 mumol/kg.min, P less than 0.01) were elevated in cirrhotics despite basal hyperinsulinemia; basal FFA oxidation was similar in cirrhotic and control subjects. With low-dose insulin infusion, plasma FFA oxidation and turnover failed to suppress normally in cirrhotics. During the two higher insulin infusion steps, all parameters of FFA metabolism suppressed normally. In summary, stable cirrhotic patients with normal glucose tolerance exhibit marked insulin resistance secondary to the impaired nonoxidative glucose disposal. Our results suggest that chronic hyperinsulinism may be responsible for the insulin resistance observed in cirrhosis.     

幽门螺旋杆菌在特发性血小板减少性紫癜发病中临床意义研究

为了探讨特发性血小板减少性紫癜（ITP）患者幽门螺旋杆菌（HP）感染的发生率及糖皮质激素联合抗HP治疗ITP的疗效，100例HP阳性ITP患者随机分为联合治疗组（根除HP及糖皮质激素治疗，n=35）、单用糖皮质激素组（n=35）和单纯抗HP组（n=30），100名健康体检者作为对照组。。结果表明：ITP组HP感染率为70％，而对照组HP感染率为56％，2组差异有显著性（p〈0．05）。联合治疗组给予根除HP及糖皮质激素治疗后，31例HP得到根除，其中23例血小板水平恢复正常，8例较治疗前升高，血小板均数为（165±225）×10^9／L，与治疗前相比有统计学意义（p〈0．01），总有效率89％，1年内复发率8％。糖皮质激素组中有2例HP自然转阴，血小板水平恢复正常，其余33例HP仍然阳性的患者中23例血小板水平未恢复正常，10例恢复正常，血小板均数为（78±26）×10^9／L，总有效率68％，1年内复发率37％。单纯抗HP组中25例肿得到根除，其中9例血小板水平恢复正常，9例较治疗前升高，血小板均数为（135±174）×10^9／L，与治疗前相比有统计学意义（p〈0．01），总有效率60％，1年内总复发率为33％。结论：ITP患者有高HP感染率，根除HP是合并HP感染的ITP患者行之有效的治疗方法，并可作为一线治疗。